Real-time nearfield acoustic holography using particle velocity.

In this paper, a series of impulse response functions between acoustic quantities on the source plane and particle velocity on the hologram plane are derived. In virtue of these functions, real-time nearfield acoustic holography (RT-NAH) is extended from pressure-based to particle velocity. Pressure, normal velocity, acceleration, and displacement radiated from planar sources can be reconstructed by measuring time-dependent particle velocity signals on the hologram plane. A simulation of an excited aluminum plate is performed to evaluate the difference in accuracy between RT-NAHs based on pressure and based on particle velocity. This study also examines the impact of impulse response functions on the reconstruction results, allowing for detailed analysis of the reconstruction accuracy based on these functions. The simulation results demonstrate that using RT-NAH based on particle velocity obtains significantly higher-accuracy reconstruction results when reconstructing normal velocity and displacement and slightly more accurate reconstructed pressure and normal acceleration.

Early outcomes, associated factors and predictive values of clinical outcomes of tandospirone in generalized anxiety disorder: a post-hoc analysis of a randomized, controlled, multicenter clinical trial.

OBJECTIVE: To examine the early outcomes, associated factors and predictive values of clinical outcomes of different tandospirone doses in patients with a generalized anxiety disorder (GAD). METHODS: This was a posthoc analysis of "a randomized, controlled multicenter clinical trial of the efficacy and safety of different doses of tandospirone on GAD". A total of 274 patients with GAD were included and randomized into the high-dose (tandospirone 60 mg/d) and low-dose (tandospirone 30 mg/d) groups for a 6-week treatment. The Hamilton Anxiety (HAMA), Clinical Global Impression-Severity (CGI-S), Short-Form-12 (SF-12) scales were used for assessment. The trial was registered at clinical trail.gov (NCT01614041). RESULTS: (1) In the first week of treatment, 35.8% of patients in the high-dose group fulfilled the early onset criteria, which was significantly higher than 19.0% found in the low-dose group (p = 0.002). In the second week of treatment, 22.6% of patients in the high-dose group achieved an early response, versus 12.4% in the low-dose group, indicating a significant difference (p = .026). (2) Factors associated with early onset at week 1 included baseline HAMA total score (OR = 0.916, 95%CI 0.882-0.952), age (OR = 0.974, 95%CI 0.950-0.998), drug dose (30 mg vs. 60 mg; OR = 0.298, 95%CI 0.156-0.568) and SF-12 physiological total score (OR = 1.030, 95%CI 1.010-1.050). (3) Early onset was significantly associated with response rate (OR = 18.34, 95%CI 12.10-27.81), remarkable response rate (OR = 27.56, 95%CI 11.65-65.17) and recovery rate (OR = 11.85, 95%CI 4.98-28.18). Group (high dose group vs. low dose group) (χ2 = 8.535, p = .003) and baseline HAMA total score (χ2 = 70.840, p < .001) were independent predictors of onset time. CONCLUSIONS: The early outcomes of high-dose tandospirone in the treatment of GAD are better than those of the low-dose group. Patients with younger age at onset, milder anxiety symptoms and better physiological functions administered high-dose tandospirone showed rapid onset, great early outcomes, high recovery rate and good prognosis. Drug onset time had a good predictive effect on treatment outcome.

The effect of the time to remission on residual symptoms and functioning among depressive patients.

OBJECTIVES: To explore the effect of time to remission on residual symptoms, functioning and quality of life (QOL) of the patients with major depressive disorder (MDD). METHOD: A total of 434 patients were enrolled from 16 sites of China. The Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR) and self-rating scales were assessed at baseline, and months 1, 3 and 6. Baseline remitters were defined as those subjects with a QIDS-SR score ≤ 5 at baseline. Later remitters was defined as those reaching remission one month (Month 1 remitters) or three month (Month 3 remitters) after baseline. Persistent non-remitters were defined as those with QIDS-SR score > 5 at all 3 assessments. A follow-up assessment was done at month 6 to examine outcomes. Cross-lagged models indicated QIDS-SR predicted social functioning and QOL. RESULTS: Totally, 179 patients at baseline achieved remission. An additional 141 participants remitted at month 1 (n = 94) or month 3 (n = 47), and 63 patients were persistent non-remitters. There were significant differences between all groups on depression severity at baseline. QOL was similar for both late remitter groups, which was better than non-remitters, but lower than early-remitters. Late remitters and non-remitters showed significant differences on change of functioning and QOL (P < 0.001) at each visit. By 6 months, all remitting groups showed lower depression severity and better social functioning and QOL than persistent non-remitters. Cross-lagged models indicated QIDS-SR predicted social functioning and QOL. CONCLUSION: We confirmed the association of earlier remission with a better quality of remission at early stage; but the time to remission does not affect future functioning and QOL.

Opposing actions of CRF-R1 and CB1 receptor on facial stimulation-induced MLI-PC plasticity in mouse cerebellar cortex.

BACKGROUND: Corticotropin-releasing factor (CRF) is the major neuromodulator orchestrating the stress response, and is secreted by neurons in various regions of the brain. Cerebellar CRF is released by afferents from inferior olivary neurons and other brainstem nuclei in response to stressful challenges, and contributes to modulation of synaptic plasticity and motor learning behavior via its receptors. We recently found that CRF modulates facial stimulation-evoked molecular layer interneuron-Purkinje cell (MLI-PC) synaptic transmission via CRF type 1 receptor (CRF-R1) in vivo in mice, suggesting that CRF modulates sensory stimulation-evoked MLI-PC synaptic plasticity. However, the mechanism of how CRF modulates MLI-PC synaptic plasticity is unclear. We investigated the effect of CRF on facial stimulation-evoked MLI-PC long-term depression (LTD) in urethane-anesthetized mice by cell-attached recording technique and pharmacological methods. RESULTS: Facial stimulation at 1 Hz induced LTD of MLI-PC synaptic transmission under control conditions, but not in the presence of CRF (100 nM). The CRF-abolished MLI-PC LTD was restored by application of a selective CRF-R1 antagonist, BMS-763,534 (200 nM), but it was not restored by application of a selective CRF-R2 antagonist, antisauvagine-30 (200 nM). Blocking cannabinoid type 1 (CB1) receptor abolished the facial stimulation-induced MLI-PC LTD, and revealed a CRF-triggered MLI-PC long-term potentiation (LTP) via CRF-R1. Notably, either inhibition of protein kinase C (PKC) with chelerythrine (5 µM) or depletion of intracellular Ca2+ with cyclopiazonic acid (100 µM), completely prevented CRF-triggered MLI-PC LTP in mouse cerebellar cortex in vivo. CONCLUSIONS: The present results indicated that CRF blocked sensory stimulation-induced opioid-dependent MLI-PC LTD by triggering MLI-PC LTP through CRF-R1/PKC and intracellular Ca2+ signaling pathway in mouse cerebellar cortex. These results suggest that activation of CRF-R1 opposes opioid-mediated cerebellar MLI-PC plasticity in vivo in mice.

SSBP1 drives high fructose-induced glomerular podocyte ferroptosis via activating DNA-PK/p53 pathway.

High fructose consumption is a significant risking factor for glomerular podocyte injury. However, the causes of high fructose-induced glomerular podocyte injury are still unclear. In this study, we reported a novel mechanism by which high fructose induced ferroptosis, a newly form of programmed cell death, in glomerular podocyte injury. We performed quantitative proteomic analysis in glomeruli of high fructose-fed rats to identify key regulating proteins involved in glomerular injury, and found that mitochondrial single-strand DNA-binding protein 1 (SSBP1) was markedly upregulated. Depletion of SSBP1 could alleviate high fructose-induced ferroptotic cell death in podocytes. Subsequently, we found that SSBP1 positively regulated a transcription factor p53 by interacting with DNA-dependent protein kinase (DNA-PK) and p53 to drive ferroptosis in high fructose-induced podocyte injury. Mechanically, SSBP1 activated DNA-PK to induce p53 phosphorylation at serine 15 (S15) to promote the nuclear accumulation of p53, and thereby inhibited expression of ferroptosis regulator solute carrier family 7 member 11 (SLC7A11) in high fructose-exposed podocytes. Natural antioxidant pterostilbene was showed to downregulate SSBP1 and then inhibit DNA-PK/p53 pathway in its alleviation of high fructose-induced glomerular podocyte ferroptosis and injury. This study identified SSBP1 as a novel intervention target against high fructose-induced podocyte ferroptosis and suggested that the suppression of SSBP1 by pterostilbene may be a potential therapy for the treatment of podocyte ferroptosis in glomerular injury.

Versatile oxalato-bridging modes: a novel three-dimensional framework structure of manganese(ii) oxalate complex [MnC2O4]·0.5H2O and the relationship with other manganese(ii) oxalates.

An unknown manganese(ii) oxalate complex [MnC2O4]·0.5H2O (1) was discovered with a novel three-dimensional structure, exhibiting versatile bridging modes of the oxalate ligand. The thermal and magnetic behaviors of this complex were studied and the relationship with four other manganese(ii) oxalates is also discussed.

Corticotrophin-Releasing Factor Modulates the Facial Stimulation-Evoked Molecular Layer Interneuron-Purkinje Cell Synaptic Transmission in vivo in Mice.

Corticotropin-releasing factor (CRF) is an important neuromodulator in central nervous system that modulates neuronal activity via its receptors during stress responses. In cerebellar cortex, CRF modulates the simple spike (SS) firing activity of Purkinje cells (PCs) has been previously demonstrated, whereas the effect of CRF on the molecular layer interneuron (MLI)-PC synaptic transmission is still unknown. In this study, we examined the effect of CRF on the facial stimulation-evoked cerebellar cortical MLI-PC synaptic transmission in urethane-anesthetized mice by in vivo cell-attached recording, neurobiotin juxtacellular labeling, immunohistochemistry techniques, and pharmacological method. Cell-attached recordings from cerebellar PCs showed that air-puff stimulation of ipsilateral whisker pad evoked a sequence of tiny parallel fiber volley (N1) followed by MLI-PC synaptic transmission (P1). Microapplication of CRF in cerebellar cortical molecular layer induced increases in amplitude of P1 and pause of SS firing. The CRF decreases in amplitude of P1 waveform were in a dose-dependent manner with the EC50 of 241 nM. The effects of CRF on amplitude of P1 and pause of SS firing were abolished by either a non-selective CRF receptor antagonist, α-helical CRF-(9-14), or a selective CRF-R1 antagonist, BMS-763534 (BMS, 200 nM), but were not prevented by a selective CRF-R2 antagonist, antisauvagine-30 (200 nM). Notably, application CRF not only induced a significant increase in spontaneous spike firing rate, but also produced a significant increase in the number of the facial stimulation-evoked action potential in MLIs. The effect of CRF on the activity of MLIs was blocked by the selective CRF-R1 antagonist, and the MLIs expressed the CRF-R1 imunoreactivity. These results indicate that CRF increases excitability of MLIs via CRF-R1, resulting in an enhancement of the facial stimulation-evoked MLI-PC synaptic transmission in vivo in mice.

Pterostilbene Improves Hepatic Lipid Accumulation via the MiR-34a/Sirt1/SREBP-1 Pathway in Fructose-Fed Rats.

High fructose intake promotes hepatic lipid accumulation. Pterostilbene, a natural analogue of resveratrol found in diet berries, exhibits a hepatoprotective property. Here, we studied the protection by pterostilbene against fructose-induced hepatic lipid accumulation and explored its possible mechanism. We observed a high expression of microRNA-34a (miR-34a, P < 0.05) and a low expression of its target, sirtuin1 (Sirt1, mRNA: P < 0.01; protein: P < 0.001), with the overactivation of downstream sterol regulatory element-binding protein-1 (SREBP-1) lipogenic pathway (nuclear SREBP-1 protein: P < 0.05; FAS and SCD1 mRNA: P < 0.01), in rat livers, as well as BRL-3A and HepG2 cells, stimulated by fructose. More interestingly, pterostilbene recovered the fructose-disturbed miR-34a expression (0.3-0.5-fold vs fructose control, P < 0.05), Sirt1 protein level (1.2- to 1.5-fold vs fructose control, P < 0.05), and SREBP-1 lipogenic pathway, resulting in significant amelioration of hepatocyte lipid accumulation in animal [hepatic triglyceride and total cholesterol (TG&TC) mg/g·wet tissue: 4.90 ± 0.19, 5.23 ± 0.16, 5.20 ± 0.29 vs fructose control 9.73 ± 1.06, P < 0.001; 3.18 ± 0.30, 3.31 ± 0.39, 3.37 ± 0.47 vs 5.67 ± 0.28, P < 0.001] and cell models (BRL-3A TG&TC mmol/g·protein: 0.123 ± 0.011 vs 0.177 ± 0.004, P < 0.001; 0.169 ± 0.011 vs 0.202 ± 0.008, P < 0.05; HepG2: 0.257 ± 0.005 vs 0.303 ± 0.016, P < 0.05; 0.143 ± 0.004 vs 0.201 ± 0.008, P < 0.001). These results provide the experimental evidence supporting the anti-lipogenic effect of pterostilbene against fructose-induced hepatic lipid accumulation via modulating the miR-34a/Sirt1/SREBP-1 pathway.

Does early and late life depression differ in residual symptoms, functioning and quality of life among the first-episode major depressive patients.

AIMS & OBJECTIVES: Age differences exist in many aspects in patients with major depressive disorder (MDD). The present study aims to examine the effect of age on treatment outcomes in first-episode MDD. METHODOLOGY: A total of 982 first-episode major depressive patients, who were above 18 years old and admitted in both psychiatric hospitals and units of general hospitals were recruited for the present study. These patients were newly treated and responded to 8-12 weeks of antidepressant treatment. Depressive symptoms, psychosocial functioning and quality of life were measured using standardized instruments. The study population was divided into three age groups: early adult (18-44 years old), middle adult (45-59 years old), and late adult (60-85 years old). RESULTS: Earlier age was associated with greater symptom severity, severer depressive symptoms in hypersomnia, concentration/decision making, negative view of the self, suicide ideation and restlessness, more impaired function, poorer satisfaction in social relationship and economic status, when compared to late adults with MDD (all P < 0.05). In the multivariable analyses, among the other variables, early age remained as an independent correlation of residual depressive severity (middle age vs. early age: OR = 0.631, 95%CI[0.462, 0.862]; old age vs. early age: OR = 0.521, 95%CI[0.348, 0.780]) and functional impairment. Comorbidity of physical illness had a negative contribution to all treatment outcomes. CONCLUSION: In first major depressive episode, early age was strongly associated with depressive severity and functional impairment after responding to antidepressant treatment. Early-life depression may be an indicator of MDD for poor clinical outcomes and high clinical burden.

Mechanisms of Etomidate-Mediated Decrease of Spontaneous Spike Activity of Mouse Cerebellar Purkinje Cells in vivo.

Etomidate is an imidazole, nonbarbiturate hypnotic agent that is increasingly used in procedural sedation. However, the effects of etomidate on the spontaneous activity of cerebellar Purkinje cells (PCs) in living mouse have not been fully understood. In this study, we investigated the effects of etomidate on the spontaneous simple spike (SS) activity of PCs in urethane-anesthetized mice by cell-attached recording and pharmacological methods. Cerebellar surface application of etomidate (50 µmol\L) reduced the SS firing rate in a concentration-dependent manner (IC50: 43.4 µmol\L). Application of either a γ-aminobutyric acid type A (GABAA) receptor antagonist, SR95531 (20 µmol\L) or a glycine receptor antagonist strychnine (10 µmol\L) significantly attenuated but not abolished the etomidate-induced decrease in PC SS firing rate. However, co-application of SR95531 (20 µmol\L) and strychnine (10 µmol\L) abolished the etomidate-induced decrease in PC SS firing rate. Moreover, intraperitoneal injection of etomidate (3 mg/kg body weight) also induced a significant depression in PC SS firing rate, which was blocked by the co-application of SR95531 and strychnine on the cerebellar surface. These results indicate that both GABAA and glycine receptors are involved in the etomidate-induced decrease in PC SS firing rate in vivo in mice.

Curcumin and allopurinol ameliorate fructose-induced hepatic inflammation in rats via miR-200a-mediated TXNIP/NLRP3 inflammasome inhibition.

Excess fructose consumption causes high prevalence of metabolic syndrome and inflammatory liver diseases. The aim of the current study was to investigate the therapeutic effects and underlying molecular mechanisms of curcumin and allopurinol in high fructose-induced hepatic inflammation. Male Sprague-Dawley rats were supplied with standard rat chow and drinking water containing 10% (w/v) fructose for consecutive 12 weeks. Curcumin (15, 30 and 60 mg/kg) and allopurinol (5 mg/kg) were administered to rats via oral gavage daily from Week 7 to 12. For in vitro experiments, curcumin (2.5 µM) and allopurinol (100 µM) were treated to 5 mM fructose-exposed Buffalo rat liver cell line (BRL-3 A) and human hepatoblastoma cell line (HepG2), respectively. The data from these animal and hepatocyte models showed that curcumin and allopurinol ameliorated fructose-induced metabolic symptom, especially hepatic inflammation in rats. Interestingly, down-regulation of microRNA-200a (miR-200a) was screened out in livers of fructose-fed rats and then validated in fructose-exposed BRL-3 A and HepG2 cells. Fructose-induced miR-200a low-expression was identified as a negative mediator of thioredoxin interacting protein (TXNIP) by direct targeting of 3'UTR-rTXNIP, subsequently activating the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome in BRL-3 A cells. Curcumin, as well as allopurinol, notably up-regulated miR-200a expression, accordingly, down-regulated TXNIP and inhibited NLRP3 inflammasome activation in fructose-fed rat livers and fructose-exposed BRL-3 A and HepG2 cells. Taken together, this study firstly identified miR-200a as a biomarker of fructose-induced hepatic inflammation, and revealed the hepatoprotection of curcumin and allopurinol via up-regulating miR-200a-mediated TXNIP/NLRP3 inflammasome pathway.

Polydatin prevents fructose-induced liver inflammation and lipid deposition through increasing miR-200a to regulate Keap1/Nrf2 pathway.

Oxidative stress is a critical factor in nonalcoholic fatty liver disease pathogenesis. MicroRNA-200a (miR-200a) is reported to target Kelch-like ECH-associated protein 1 (Keap1), which regulates nuclear factor erythroid 2-related factor 2 (Nrf2) anti-oxidant pathway. Polydatin (3,4',5-trihydroxy-stilbene-3-ß-D-glucoside), a polyphenol found in the rhizome of Polygonum cuspidatum, have anti-oxidative, anti-inflammatory and anti-hyperlipidemic effects. However, whether miR-200a controls Keap1/Nrf2 pathway in fructose-induced liver inflammation and lipid deposition and the blockade of polydatin are still not clear. Here, we detected miR-200a down-regulation, Keap1 up-regulation, Nrf2 antioxidant pathway inactivation, ROS-driven thioredoxin-interacting protein (TXNIP) over-expression, NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) inflammasome activation and dysregulation of peroxisome proliferator activated receptor-α (PPAR-α), carnitine palmitoyl transferase-1 (CPT-1), sterol regulatory element binging protein 1 (SREBP-1) and stearoyl-CoA desaturase-1 (SCD-1) in rat livers, BRL-3A and HepG2 cells under high fructose induction. Furthermore, the data from the treatment or transfection of miR-200a minic, Keap1 and TXNIP siRNA, Nrf2 activator and ROS inhibitor demonstrated that fructose-induced miR-200a low-expression increased Keap1 to block Nrf2 antioxidant pathway, and then enhanced ROS-driven TXNIP to activate NLRP3 inflammasome and disturb lipid metabolism-related proteins, causing inflammation and lipid deposition in BRL-3A cells. We also found that polydatin up-regulated miR-200a to inhibit Keap1 and activate Nrf2 antioxidant pathway, resulting in attenuation of these disturbances in these animal and cell models. These findings provide a novel pathological mechanism of fructose-induced redox status imbalance and suggest that the enhancement of miR-200a to control Keap1/Nrf2 pathway by polydatin is a therapeutic strategy for fructose-associated liver inflammation and lipid deposition.

Comparison of residual depressive symptoms and functional impairment between fully and partially remitted patients with major depressive disorder: a multicenter study.

This study compared residual depressive and somatic symptoms and functional impairment between remitted and partially remitted patients with major depressive disorder (MDD), and explored the associations of functioning with demographic and clinical characteristics including residual depressive symptoms. Altogether, 1503 outpatients with MDD formed the study sample. Residual symptoms and psychosocial functioning were measured using standardized instruments. Approximately half (51.2%) of the patients who responded to antidepressant treatment achieved remission ('remitters'), while the rest who responded to treatment achieved only partial remission ('non-remitters'). Residual mood symptoms in remitters included sleep disturbances (66.6%), fatigue (32.3%), decreased concentration (31.3%), appetite/weight disturbances (28.8%), psychomotor changes (23.2%), sad mood (21.9%) and loss of interest (21.1%) measured by the Quick Inventory of Depressive Symptomatology-Self-Report. Residual somatic symptoms included headache (31.9%), intestinal complaints (31.3%), heart pounding/racing (26.3%), gastric complaints (22.3%), dizziness (22.2%) and stomach pain (20.6%) measured by the Patient Health Questionnaire-15. Such residual symptoms were even more frequent in the 'non-remitters' group. Residual symptoms of fatigue, psychomotor changes, sleep disturbance and appetite/weight disturbance contributed to impairment of all functional domains. Given the negative impact of residual symptoms on psychosocial functioning, more attention needs to be paid to the assessment and treatment of residual depressive symptoms.

[Analysis of Cut-off Value in Screening of Thalassemia by Capillary Hemoglobin Electrophoresis for Pregnant Women from Shenzhen Region of China].

OBJECTIVE: To investigate the cut-off value in screening of thalassemia in pregnant women from Shenzhen region by capillary hemoglobin electrophoresis. METHODS: The data of capillary hemoglobin electrophoresis and genetic diagnosis of thalassemia from 2122 examined prenatal women were retrospectively analyzed. Capillary hemoglobin electrophoresis and α-, ß- genetic diagnosis of thalassemia were carried out for every woman. Hemoglobin electrophoresis was performed using Capillarys 2 full-automated electrophoresis instrument. Gap polymerase chain reaction and reverse dot blot were used for genetic diagnosis of thalassemia genotyping test. The cut-off value in screening of thalassemia was determined by receiver operating characteristic curve and next to analyze the value of HbA2 and HbF in screening of thalassemia using the decided cut-off value. RESULTS: The areas under the curve (AUC(Roc)) of HbA2 for diagnosis of α-, ß- thalassemia were 0.75 and 0.981 respectively, and the AUC(Roc) of HbF for diagnosis of ß-thalassemia was 0.787. When HbA2 ≤ 2.55 was taken as the cut-off value of HbA2 for diagnosis of α-thalassemia, the sensitivity, specificity, positive likelihood ratio (LR(+)) and negative likelihood ratio (LR(-)) were 89.5%, 54.8%, 1.98, 0.19 respectively. When HbA2 ≥3.9 was taken as the cut off value of HbA2 for diagnosis of ß-thalassemia, the sensitivity, specificity, LR(+) and LR(-) were 96.1%, 99.8% 480.5, 0.04 respectively. When HbF ≥0.75 was taken as the cut off value of HbF for diagnosis of ß-thalassemia, the sensitivity, specificity, LR(+) and LR(-) were 83.6%, 61.8% respectively. CONCLUSION: The cut-off value in screening of thalassemia by capillarys 2 full automated electrophoresis instrument is different from that of the traditional method of hemoglobin electrophoresis, such as cellulose acetate membrane electrophoresis and agarose gel electrophoresis. Each laboratory should establish their own respective cut off value.

Investigation of Y/SBA Composite Molecular Sieves Morphology Control and Catalytic Performance for n-Pentane Aromatization.

Using Y molecular sieve as the core, Y/SBA-15 composite molecular sieves were prepared by different crystallization methods in the paper. The growth process and morphologies of the composite molecular sieves were controlled by adjusting the synthesis factors. The structures and acidity of two kinds of composite molecular sieves were characterized by X-ray diffraction (XRD), N2 adsorption/desorption, transmission electron microscopy (TEM), and NH3-TPD. The catalysis performances of the composite molecular sieves were investigated in the aromatization reaction of n-pentane. The results indicated that the desired core-shell composite molecular sieves were obtained when the crystallization conditions were 36 hours, 100 °C and secondary crystallization. The aromatization results showed that core-shell composite molecular sieves had better selectivity for producing high application value xylenes compared to mixed-crystal composite molecular sieves.

Peripheral Templation Generates an M(II) 6 L4 Guest-Binding Capsule.

Pseudo-octahedral M(II) 6 L4 capsules result from the subcomponent self-assembly of 2-formylphenanthroline, threefold-symmetric triamines, and octahedral metal ions. Whereas neutral tetrahedral guests and most of the anions investigated were observed to bind within the central cavity, tetraphenylborate anions bound on the outside, with one phenyl ring pointing into the cavity. This binding configuration is promoted by the complementary arrangement of the phenyl rings of the intercalated guest between the phenanthroline units of the host. The peripherally bound, rapidly exchanging tetraphenylborate anions were found to template an otherwise inaccessible capsular structure in a manner usually associated with slow-exchanging, centrally bound agents. Once formed, this cage was able to bind guests in its central cavity.

Up-regulated fractalkine (FKN) and its receptor CX3CR1 are involved in fructose-induced neuroinflammation: Suppression by curcumin.

Recent studies suggest that diet-induced fractalkine (FKN) stimulates neuroinflammation in animal models of obesity, yet how it occurs is unclear. This study investigated the role of FKN and it receptor, CX3CR1, in fructose-induced neuroinflammation, and examined curcumin's beneficial effect. Fructose feeding was found to induce hippocampal microglia activation with neuroinflammation through the activation of the Toll-like receptor 4 (TLR4)/nuclear transcription factor κB (NF-κB) signaling, resulting in the reduction of neurogenesis in the dentate gyrus (DG) of mice. Serum FKN levels, as well as hypothalamic FKN and CX3CR1 gene expression, were significantly increased in fructose-fed mice with hypothalamic microglia activation. Hippocampal gene expression of FKN and CX3CR1 was also up-regulated at 14d and normalized at 56d in mice fed with fructose, which were consistent with the change of GFAP. Furthermore, immunostaining showed that GFAP and FKN expression was increased in cornu amonis 1, but decreased in DG in fructose-fed mice. In vitro studies showed that GFAP and FKN expression was stimulated in astrocytes, and suppressed in mixed glial cells exposed to 48h-fructose, with the continual increase of pro-inflammatory cytokines. Thus, increased FKN and CX3CR1 may cause a cross-talk between activated glial cells and neurons, playing an important role in the development of neuroinflammation in fructose-fed mice. Curcumin protected against neuronal damage in hippocampal DG of fructose-fed mice by inhibiting microglia activation and suppressed FKN/CX3CR1 up-regulation in the neuronal network. These results suggest a new therapeutic approach to protect against neuronal damage associated with dietary obesity-associated neuroinflammation.

[Quality characteristics of human spermatozoa with hyaluronic acid receptors].

OBJECTIVE: To analyze the quality characteristics of human spermatozoa with hyaluronic acid (HA) receptors and search for a new indicator for the assessment of sperm quality. METHODS: Using sperm-HA binding assay with HA-coated slides, we determined the binding rate of motile sperm with HA receptors and analyzed its correlation with routine semen parameters, sperm membrane function, sperm fertilizing function and diminished/arrested sperm maturation. RESULTS: The motile sperm with HA binding sites in the acrosomal region showed significantly higher acrosomal integrity ([95.4 +/- 3.9]%) and mitochondrial membrane potential (MMP) ([97.8 +/- 2.1]%) than those in the initial semen ([68.8 +/- 6.2]% and [72.8 +/- 7.4]%) (P < 0.01). The sperm-HA binding scores were correlated mildly with many routine semen parameters (r = 0.195-0.268, P < 0.05), positively with the acrosome reaction level after ionophore challenge (r = 0.666, P < 0.01) and normal sperm morphology (r = 0.417, P < 0.01), and negatively with sperm nucleoprotein immaturation (r = -0.266, P < 0.01), DNA fragmentation (r = -0. 308, P < 0.01) and excessive residual cytoplasm (r = -0.218, P < 0.05). CONCLUSION: Sperm with HA receptors in the acrosomal region exhibit significant advantages in plasma membrane structure, fertilizing potential and maturation. The sperm-HA binding assay, which is based on a relationship between sperm receptors for zona pellucida and HA, is likely to become a new independent indicator for assessing the multiple qualities of spermatozoa.